PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8906568-2 1996 Depletion of extracellular Ca2+ abolished the Cch-mediated phospholipase D (PLD) activation, indicating the requirement of Ca2+ influx. Carbachol 46-49 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 76-79 15548524-11 2005 The expression of the tubulin binding region of PLD2 blocked the later decrease in carbachol-induced PLD activity by masking tubulin binding. Carbachol 83-92 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 48-51 15255942-0 2004 Role of phospholipase D signaling in ethanol-induced inhibition of carbachol-stimulated DNA synthesis of 1321N1 astrocytoma cells. Carbachol 67-76 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 8-23 15255942-4 2004 1-Butanol, which is a substrate for PLD and inhibits PA formation, inhibited carbachol-induced cell proliferation and the underlying intracellular signaling, whereas its analog tert-butanol, which is a poor substrate for PLD, was much less effective. Carbachol 77-86 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 36-39 15255942-7 2004 Taken together, these results indicate that PLD activation plays an important role in carbachol-induced astroglial cell proliferation by generating the second messenger PA, which activates PKC zeta. Carbachol 86-95 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 44-47 15255942-8 2004 Moreover, the effect of ethanol on carbachol-induced proliferation appears to be mediated, at least in part, by its ability to interact with PLD leading to a decreased synthesis of PA. Carbachol 35-44 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 141-144 15087463-4 2004 Cellular PLD activity was increased in response to a variety of secretagogues including the nutrient glucose and the cholinergic receptor agonist carbamoylcholine. Carbachol 146-162 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 9-12 15020229-5 2004 Glutamate was a potent activator of PLD in neurons but not in astrocytes, whereas noradrenaline and carbachol increased PLD activity only in astrocytes. Carbachol 100-109 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 120-123 11245595-0 2001 PLD pathway involved in carbachol-induced Cl- secretion: possible role of TNF-alpha. Carbachol 24-33 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 11245595-5 2001 The aim of the present study was to investigate whether the phospholipase D (PLD) pathway plays a role in the carbachol response and the potentiating effect of TNF-alpha. Carbachol 110-119 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 60-75 11245595-5 2001 The aim of the present study was to investigate whether the phospholipase D (PLD) pathway plays a role in the carbachol response and the potentiating effect of TNF-alpha. Carbachol 110-119 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 77-80 1331066-3 1992 Carbachol-mediated activation of the Hm1 receptor in the 39M1-81 clone, which is not a mitogenic signal, produced a similarly rapid although greater activation of PLD. Carbachol 0-9 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 163-166 7650010-1 1995 mAChR-stimulated PLD was turned off after 2 min of receptor activation with either the full (carbachol) or partial agonist (pilocarpine) and remained completely suppressed for at least 4 h. Partial recovery was observed 24 h after agonist removal. Carbachol 93-102 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 17-20 7935319-6 1994 In addition, cells pretreated with carbachol or thrombin show a normal response to phorbol-12-myristate-13-acetate, suggesting that the enzymatic activity of PLD is not compromised. Carbachol 35-44 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 158-161 1331066-5 1992 In each case, the stimulation of PLD correlated closely with the ability to stimulate inositol phospholipid breakdown and was entirely dependent on the activation of protein kinase C. Moreover, the ability of both thrombin and carbachol to stimulate PLD was found to be rapidly desensitized, with a similar time course of desensitization (t1/2 desensitization, 90 s). Carbachol 227-236 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 33-36 1331066-5 1992 In each case, the stimulation of PLD correlated closely with the ability to stimulate inositol phospholipid breakdown and was entirely dependent on the activation of protein kinase C. Moreover, the ability of both thrombin and carbachol to stimulate PLD was found to be rapidly desensitized, with a similar time course of desensitization (t1/2 desensitization, 90 s). Carbachol 227-236 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 250-253 1331066-7 1992 In this regard, in addition to stimulation of PLD, thrombin and carbachol were both able to stimulate the activity of a phosphocholine-specific phospholipase C (PC-PLC), which did not appear to desensitize within the time course employed. Carbachol 64-73 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 46-49 2002344-3 1991 In addition, in the presence of ethanol (170-300 mM), CCh elevated levels of [3H]PEt [which is regarded as a specific indicator of phospholipase D (PLD) activity] by three- to sixfold. Carbachol 54-57 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 131-146 2002344-3 1991 In addition, in the presence of ethanol (170-300 mM), CCh elevated levels of [3H]PEt [which is regarded as a specific indicator of phospholipase D (PLD) activity] by three- to sixfold. Carbachol 54-57 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 148-151 2176212-6 1990 Treatment of 1321N1 cells with carbachol results in increases in radiolabeled choline, phosphatidic acid (PA) and phosphatidylethanol (PEt), metabolites that are products of phospholipase D (PLD) action on PC. Carbachol 31-40 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 174-189 2176212-6 1990 Treatment of 1321N1 cells with carbachol results in increases in radiolabeled choline, phosphatidic acid (PA) and phosphatidylethanol (PEt), metabolites that are products of phospholipase D (PLD) action on PC. Carbachol 31-40 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 191-194 2176212-9 1990 It appears that most of the DG is formed through the action of PLD, since propranolol (which inhibits the conversion of PA to DG) and down-regulation of protein kinase C (which prevents activation of PLD by carbachol) both markedly inhibit DG production. Carbachol 207-216 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 63-66 2176212-9 1990 It appears that most of the DG is formed through the action of PLD, since propranolol (which inhibits the conversion of PA to DG) and down-regulation of protein kinase C (which prevents activation of PLD by carbachol) both markedly inhibit DG production. Carbachol 207-216 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 200-203 2176212-10 1990 Using a protocol in which cells are stimulated with carbachol for only one minute (a period during which PLD and PA formation are maximally activated), we show that DG mass continues to increase following removal of agonist. Carbachol 52-61 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 105-108 2130511-18 1990 Activation of phospholipase D (PLD) was demonstrated by the finding that phosphatidic acid increased in response to PMA or carbachol prior to the increase in PA. Carbachol 123-132 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 14-29 2130511-18 1990 Activation of phospholipase D (PLD) was demonstrated by the finding that phosphatidic acid increased in response to PMA or carbachol prior to the increase in PA. Carbachol 123-132 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 31-34